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Abstract
Rebreathing may impair ventilation and lead to sudden death among sleeping infants. To estimate the potential for rebreathing imposed by an infant's sleep microenvironment, we developed a mechanical model to assess the rate of CO2 dispersal away from an infant's face. We compared the mechanical model results with changes in arterial blood gases of rabbits. The rabbits breathed into the same microenvironments used for the model studies. In the rabbits, rebreathing (documented by capnometry) caused hypercarbia and in some cases death. The mechanical model consisted of the mannequin head positioned as in the rabbit studies and connected to a 100-ml syringe filled with CO2. CO2 was washed out of the system using 30-ml "breaths" (rate = 15/min). The half times (t1/2) for CO2 dispersal served to quantify the rebreathing potential of 16 items of bedding. The t1/2 values correlated with increments in the rabbits' arterial PCO2 (r = 0.789). The threshold for the increase in the rabbits' arterial PCO2 corresponded to t1/2 values of > or = 18.7 s; the 90% point for lethality in the rabbit model was 28.1 s. The mechanical model was also used to show the independent effects of softness and porosity of bedding on its rebreathing potential. By describing the potential for rebreathing within bedding, the mechanical model should be useful in future quantitative studies of infants' respiratory adaptation to sleep microenvironments.
... A mechanical model was used to quantify the rebreathing potential of each sleep surface. 32 The model used an infant mannequin, with its head weighted to approximate the density of human tissue. The nares were connected via tubing to a 100-mL reservoir and piston pump. ...
... To determine whether the sleep systems would significantly limit CO 2 dispersal, the results were compared with the control t 1/2 and with t 1/2 thresholds associated with the onset of rebreathing (t 1/2 Ͼ 21.1 seconds) and lethal rebreathing (t 1/2 Ͼ 24.0 seconds) in a rabbit model. 32 Statistical comparisons were completed using analysis of variance with post-hoc Dunnett's test for multiple comparisons against a single control. 35 Differences were considered significant if P was Ͻ.05. ...
... The top solid line at 24.0 seconds represents the washout t 1/2 at which lethality occurred in animal studies. 32 The middle line at 21.l seconds is the t 1/2 at which there was a rise in Paco 2 in animal studies. 32 The lowest line at 13.4 seconds is the control, face-to-side washout t 1 ⁄2. ...
Rebreathing of exhaled air is one proposed mechanism for the increased risk for sudden infant death syndrome among prone sleeping infants. We evaluated how carbon dioxide (CO(2)) dispersal was affected by a conventional crib mattress and 5 products recently marketed to prevent prone rebreathing.
Infant pulmonary laboratory. EQUIPMENT: An infant mannequin with its nares connected via tubing to an 100-mL reservoir filled with 5% CO(2). The sleep surfaces studied included: firm mattress covered by a sheet, Bumpa Bed, Breathe Easy, Kid Safe/Baby Air, Halo Sleep System, and Sleep Guardian. The mannequin was positioned prone face-down or near-face-down. The sleep surfaces were studied with the covering sheet taut, covering sheet wrinkled, and with the mannequin arm positioned up, near the face.
. We measured the fall in percentage end-tidal CO(2) as the reservoir was ventilated with the piston pump. The half-time for CO(2) dispersal (t(1/2)) is an index of the ability to cause or prevent rebreathing.
Compared with the face-to-side control, 5 of 6 surfaces allowed a significant increase in t(1/2) in all 3 prone scenarios. The firm mattress and 4 of the 5 surfaces designed to prevent rebreathing consistently allowed t(1/2) above thresholds for the onset of CO(2) retention and lethal rebreathing in an animal model (J Appl Physiol. 1995;78:740).
With very few exceptions, infants should be placed supine for sleep. For infants placed prone or rolling to the prone position, significant rebreathing of exhaled air would be likely on all surfaces studied, except one.
... However, according to the recent epidemiological reports, the SIDS risk associated with side position is similar or even higher than that associated with supine position [5,6]. The experimental investigation also shows the risk of rebreathing expired carbon dioxide (CO 2 ) can be elevated for the infants sleeping with face-to-side position [7]. Accordingly, the APP no longer recognizes side position as a reasonable alternative to supine position [8]. ...
... Table 5 compares the results of SVE3, SVE4, SVE3*, ε P and influenza quanta concentration in the inhalation. In Case 1 with- out using WCPV, SVE3 was slightly greater in the inhalation of the side sleep infant, consistent with the experimental findings that the side position had the potential to increase the risk of SIDS due to the rebreathing of exhaled CO 2 [7]. In Case 2 with WCPV-75 • , SVE3 slightly decreased for the side sleep infant as personalized air covered the whole head with a relatively uniform distribution. ...
... However, this also highlights the subtleties of infant and bedding positioning, which are not immediately visible and may allow some infants to sleep facedown, whereas others who do so may experience dangerous asphyxia. Although we investigated only one type of bedding, it is conceivable that certain characteristics of the composition of the bedding influence the occurrence and size of channels and thereby would be relevant to its safety for infants (26). ...
... Reasons for formation of gradients are not clearly identified. We theorize that the microstructure of the bedding (23,24,26) allows airflow with minimal turbulence and consequently little air mixing. Also, exchange of gases at the interface between the bedding and the environment must be occurring by diffusion. ...
Some infants sleep facedown for long periods with no ill effects, whereas others become hypoxemic. Rebreathing of expired air has been determined by CO(2) measurement; however, O(2) levels under such conditions have not been determined. To evaluate this and other factors influencing inspired gas concentrations, we studied 21 healthy infants during natural sleep while facedown on soft bedding. We measured gas exchange with the environment and bedding, ventilatory response to rebreathing, and concentrations of inspired CO(2) and O(2). Two important factors influencing inspired gas concentrations were 1) a variable seal between bedding and infants' faces and 2) gas gradients in the bedding beneath the infants, with O(2)-poor and CO(2)-rich air nearest to the face, fresher air distal to the face, and larger tidal volumes being associated with fresher inspired air. Minute ventilation increased significantly while rebreathing because of an increase in tidal volume, not frequency. The measured drop in inspired O(2) was significantly greater than the accompanying rise in inspired CO(2). This appears to be due to effects of the respiratory exchange ratio and differential tissue solubilities of CO(2) and O(2) during unsteady conditions.
... It may seem counterintuitive to place infants with respiratory distress in the prone position, because it has been shown to increase the risk of rebreathing exhaled gases, which can result in hypoxia or hypercarbia. [98][99][100][101] The prone position decreases the rate of heat loss and increases body temperature, putting the infant at risk for overheating. 102,103 Prone positioning has been shown to alter autonomic regulation of the cardiovascular system, especially in preterm infants, potentially decreasing cerebral oxygenation. ...
Of the nearly 3.8 million infants born in the United States in 2018, 8.3% had low birth weight (<2500 g [5.5 lb]) and 10% were born preterm (gestational age of <37 completed weeks). Many of these infants and others with congenital anomalies, perinatally acquired infections, and other disease require admission to a NICU. In the past decade, admission rates to NICUs have been increasing; it is estimated that between 10% and 15% of infants will spend time in a NICU, representing approximately 500 000 neonates annually. Approximately 3600 infants die annually in the United States from sleep-related deaths, including sudden infant death syndrome International Classification of Diseases, 10th Revision (R95), ill-defined deaths (R99), and accidental suffocation and strangulation in bed (W75). Preterm and low birth weight infants are particularly vulnerable, with an incidence of death 2 to 3 times greater than healthy term infants. Thus, it is important for health care professionals to prepare families to maintain their infant in a safe sleep environment, as per the recommendations of the American Academy of Pediatrics. However, infants in the NICU setting commonly require care that is inconsistent with infant sleep safety recommendations. The conflicting needs of the NICU infant with the necessity to provide a safe sleep environment before hospital discharge can create confusion for providers and distress for families. This technical report is intended to assist in the establishment of appropriate NICU protocols to achieve a consistent approach to transitioning NICU infants to a safe sleep environment as soon as medically possible, well before hospital discharge.
... Of the various hypotheses associated with prone sleeping, a leading one is that expired gas is somehow trapped in the vicinity of the nostrils and re-inspired or "rebreathed" (7,8,10,12,14,15,33,34,39,40), acting as a "stressor" (17). The gas has a high CO 2 concentration that displaces O 2 , causing death that is triggered by asphyxia due to the inability of the infant to extricate himself/herself from the dangerous high-CO 2 /low-O 2 environment (19,23,24,33). Various commercial products have been developed and tested with a view toward reducing or eliminating rebreathing (4,11). ...
The rebreathing of expired air, with high carbon dioxide and low oxygen concentrations, has long been implicated in unexplained Sudden Infant Death Syndrome (SIDS) when infants are placed to sleep in a prone (facedown) position. This study elucidates the effect of aerodynamic parameters: Reynolds number, Strouhal number and Froude number, on the percentage of expired air that is re-inspired (rebreathed). A nasal module was designed that served as a simplified geometric representation of infant nostrils and placed above a hard flat surface. Quantitative and flow visualization experiments were performed to measure rebreathing, using water as the working medium, under conditions of dynamic similarity. Different anatomical (e.g. tidal volume, nostril diameter), physiological (e.g. breathing frequency) and environmental (e.g. temperature, distance from the surface) factors were considered. Increases in Strouhal number (simultaneously faster and shallower breathing), always produced higher rebreathed percentages, because rolled-up vortices in the vicinity of the nostrils had less time to move away by self-induction. Positively and negatively buoyant flows resulted in significant rebreathing. In the latter case, consistent with a warm environment and a high percentage of rebreathed CO2, denser gas pooled in the vicinity of the nostrils. Reynolds numbers below 200 also dramatically increased rebreathing because the expired gas pooled much closer to the nostrils. These results clearly elucidated how the prone position dramatically increases rebreathing by a number of different mechanisms. Furthermore, the results offer plausible explanations of why a high temperature environment and low birthweight are SIDS risk factors.
... The prone or side sleep position can increase the risk of rebreathing expired gases, resulting in hypercapnia and hypoxia. [54][55][56][57] The prone position also increases the risk of overheating by decreasing the rate of heat loss and increasing body temperature compared with infants sleeping supine. 58,59 Recent evidence suggests that prone sleeping alters the autonomic control of the infant cardiovascular system during sleep, particularly at 2 to 3 months of age, 60 and can result in decreased cerebral oxygenation. ...
... Supine positioning for every sleep is the most important intervention to reduce the risk of SIDS. Prone positioning is not recommended because it poses an increased risk for hypoxia and hypercapnia because of rebreathing, [14][15][16][17] an increased risk for overheating, 18 , 19 a decrease in cerebral oxygenation because of changes in autonomic control of the cardiovascular system, 20 , 21 and an increased arousal threshold. 22 Additional recommendations focus on reducing the risk of other SUIDs, including entrapment and suffocation. ...
Background:
More than 95% of higher-order multiples are born preterm and more than 90% are low birth weight, making this group of infants especially vulnerable to sudden infant death syndrome (SIDS). Emerging evidence suggests that families with twins face challenges adhering to the American Academy of Pediatrics (AAP) recommendations to reduce SIDS risks. Adherence to the AAP recommendations in families with higher-order multiples has not been described.
Purpose:
This study describes SIDS risk reduction infant care practices for higher-order multiples during the first year of life.
Methods:
Mothers caring for higher-order multiple-birth infants were recruited from an online support group. An online survey was used to assess infant care practices when the infants were first brought home from the hospital as well as at the time of the survey.
Results:
Ten mothers of triplets and 4 mothers of quadruplets responded. Less than 80% of the mothers practiced "back to sleep" immediately postdischarge. Supine sleep positioning decreased over time, particularly during daytime naps. Only 50% of the infants shared the parents' bedroom and approximately 30% bed-shared with their siblings. Sleep-time pacifier use was low.
Implications for practice:
Safe sleep education must include specific questions regarding home sleeping arrangements, encouragement of breast milk feedings, supine positioning, and pacifier use at every sleep for higher-order multiple infants well before discharge in order for parents to plan a safe sleep environment at home.
Implications for research:
Prospective studies to identify barriers and facilitators can inform future strategies supporting adherence to safe sleep practices for higher-order multiple infants.
... The prone or side sleep position can increase the risk of rebreathing expired gases, resulting in hypercapnia and hypoxia. [54][55][56][57] The prone position also increases the risk of overheating by decreasing the rate of heat loss and increasing body temperature compared with infants sleeping supine. 58,59 Recent evidence suggests that prone sleeping alters the autonomic control of the infant cardiovascular system during sleep, particularly at 2 to 3 months of age, 60 and can result in decreased cerebral oxygenation. ...
Despite a major decrease in the incidence of sudden infant death syndrome (SIDS) since the American Academy of Pediatrics (AAP) released its recommendation in 1992 that infants be placed for sleep in a nonprone position, this decline has plateaued in recent years. Concurrently, other causes of sudden unexpected infant death occurring during sleep (sleep-related deaths), including suffocation, asphyxia, and entrapment, and ill-defined or unspecified causes of death have increased in incidence, particularly since the AAP published its last statement on SIDS in 2005. It has become increasingly important to address these other causes of sleep-related infant death. Many of the modifiable and nonmodifiable risk factors for SIDS and suffocation are strikingly similar. The AAP, therefore, is expanding its recommendations from being only SIDS-focused to focusing on a safe sleep environment that can reduce the risk of all sleep-related infant deaths including SIDS. The recommendations described in this report include supine positioning, use of a firm sleep surface, breastfeeding, room-sharing without bed-sharing, routine immunization, consideration of a pacifier, and avoidance of soft bedding, overheating, and exposure to tobacco smoke, alcohol, and illicit drugs. The rationale for these recommendations is discussed in detail in this technical report. The recommendations are published in the accompanying "Policy Statement--Sudden Infant Death Syndrome and Other Sleep-Related Infant Deaths: Expansion of Recommendations for a Safe Infant Sleeping Environment," which is included in this issue (www.pediatrics.org/cgi/doi/10.1542/peds.2011-2220).
Every year in the United States, approimately 3500 infants die of sleep-related infant deaths, including sudden infant death syndrome (SIDS) (International Statistical Classification of Diseases and Related Health Problems 10th Revision [ICD-10] R95), ill-defined deaths (ICD-10 R99), and accidental suffocation and strangulation in bed (ICD-10 W75). After a substantial decline in sleep-related deaths in the 1990s, the overall death rate attributable to sleep-related infant deaths have remained stagnant since 2000, and disparities persist. The triple risk model proposes that SIDS occurs when an infant with intrinsic vulnerability (often manifested by impaired arousal, cardiorespiratory, and/or autonomic responses) undergoes an exogenous trigger event (eg, exposure to an unsafe sleeping environment) during a critical developmental period. The American Academy of Pediatrics recommends a safe sleep environment to reduce the risk of all sleep-related deaths. This includes supine positioning; use of a firm, noninclined sleep surface; room sharing without bed sharing; and avoidance of soft bedding and overheating. Additional recommendations for SIDS risk reduction include human milk feeding; avoidance of exposure to nicotine, alcohol, marijuana, opioids, and illicit drugs; routine immunization; and use of a pacifier. New recommendations are presented regarding noninclined sleep surfaces, short-term emergency sleep locations, use of cardboard boxes as a sleep location, bed sharing, substance use, home cardiorespiratory monitors, and tummy time. In addition, additional information to assist parents, physicians, and nonphysician clinicians in assessing the risk of specific bed-sharing situations is included. The recommendations and strength of evidence for each recommendation are published in the accompanying policy statement, which is included in this issue.
Of the nearly 3.8 million infants born in the United States in 2018, 8.3% had low birth weight (ie, weight <2500 g) and 10% were born preterm (ie, gestational age of <37 weeks). Ten to fifteen percent of infants (approximately 500 000 annually), including low birth weight and preterm infants and others with congenital anomalies, perinatally acquired infections, and other diseases, require admission to a NICU. Every year, approximately 3600 infants in the United States die of sudden unexpected infant death (SUID), including sudden infant death syndrome (SIDS), unknown and undetermined causes, and accidental suffocation and strangulation in an unsafe sleep environment. Preterm and low birth weight infants are 2 to 3 times more likely than healthy term infants to die suddenly and unexpectedly. Thus, it is important that health care professionals prepare families to maintain their infant in a safe home sleep environment as per recommendations of the American Academy of Pediatrics. Medical needs of the NICU infant often require practices such as nonsupine positioning, which should be transitioned as soon as medically possible and well before hospital discharge to sleep practices that are safe and appropriate for the home environment. This clinical report outlines the establishment of appropriate NICU protocols for the timely transition of these infants to a safe home sleep environment. The rationale for these recommendations is discussed in the accompanying technical report "Transition to a Safe Home Sleep Environment for the NICU Patient," included in this issue of Pediatrics.
Infants born before 32 weeks gestational age and receiving respiratory support at 36 weeks postmenstrual age (PMA) are diagnosed with bronchopulmonary dysplasia. This label suggests that their need for supplemental oxygen (O2) is primarily due to acquired dysplasia of airways and airspaces, and that the supplemental O2 is treating residual parenchymal lung disease. However, emerging evidence suggests that immature ventilatory control may also contribute to the need for supplemental O2 at 36 weeks PMA.
In all newborns, maturation of ventilatory control continues ex utero and is a plastic process. Among premature infants, supplemental O2 mitigates the hypoxemic effects of delayed maturation of ventilatory control, as well as reduces the duration and frequency of periodic breathing events.
Nevertheless, prematurity is associated with altered and occasionally aberrant maturation of ventilatory control. Infants born prematurely, with or without a diagnosis of BPD, are more prone to long-lasting effects of dysfunctional ventilatory control.
This review addresses normal and abnormal maturation of ventilatory control and suggests how aberrant maturation complicates assigning the diagnosis of bronchopulmonary dysplasia. Greater awareness of the interaction between parenchymal lung disease and delayed maturation of ventilatory control is essential to understanding why a given premature infant requires and is benefitting from supplemental O2 at 36 weeks PMA.
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Supine (back) sleeping has been shown to decrease the incidence of SIDS and SUID (sleep-related infant deaths). Despite recommendations to place infants in the supine position for sleep, parents sometimes choose the non-supine position for their infants. This choice can be related to parental attitudes about supine sleep for their infants, perception about social norms, and whether they have control over which position their infants are placed to sleep. Health-care providers can get more infants in the supine position to sleep by consistently recommending and modeling the supine sleep position and by addressing parental concerns.
Investigation of Sudden Infant Death Syndrome - edited by Marta C. Cohen June 2019
When infants die suddenly and unexpectedly, the causes can be effectively considered using a triple risk model of individual infant susceptibility, developmental vulnerability, and environmental stressors. Sleep practices, particularly prone sleeping and bed sharing, increase the risk posed to vulnerable infants by environmental factors.
Infants born prematurely are at increased risk for sudden unexpected death, most likely because of immaturity of respiratory control that causes hypoxemia and long apneas.
Infants coming to an emergency department because of a possible cardiorespiratory event that was worrisome to a caregiver should be managed along a spectrum that includes reassurance but is informed by an awareness of potentially serious problems presenting as a nonlethal event.
Sudden Infant Death Syndrome (SIDS) is an overly broad classification bin for sudden unexplained infant deaths. SIDS has become a “diagnostic” phrase that encompasses unidentified, disease-related causes of death, deaths likely due to accidental asphyxia, and possibly unrecognized homicides. There is a prevailing false concept that SIDS is a “real” and discrete diagnostic entity rather than a phrase that signifies an inability to state why an infant has died. This has been perpetuated by the International Statistical Classification of Diseases and Related Health Problems (ICD-10), which recognizes SIDS as a “cause” of death. We propose simplified, unambiguous language for the death certificate in cases of sudden unexplained infant death. We propose changes to ICD-10 nomenclature and vital statistics tabulation practices of the National Center for Health Statistics (a division of the Centers for Disease Control and Prevention) to end the use of SIDS as a diagnosis.
Approximately 3500 infants die annually in the United States from sleep-related infant deaths, including sudden infant death syndrome (SIDS), ill-defined deaths, and accidental suffocation and strangulation in bed. After an initial decrease in the 1990s, the overall sleep-related infant death rate has not declined in more recent years. Many of the modifiable and nonmodifiable risk factors for SIDS and other sleep-related infant deaths are strikingly similar. The American Academy of Pediatrics recommends a safe sleep environment that can reduce the risk of all sleep-related infant deaths. Recommendations for a safe sleep environment include supine positioning, use of a firm sleep surface, room-sharing without bed-sharing, and avoidance of soft bedding and overheating. Additional recommendations for SIDS risk reduction include avoidance of exposure to smoke, alcohol, and illicit drugs; breastfeeding; routine immunization; and use of a pacifier. New evidence and rationale for recommendations are presented for skin-to-skin care for newborn infants, bedside and in-bed sleepers, sleeping on couches/armchairs and in sitting devices, and use of soft bedding after 4 months of age. In addition, expanded recommendations for infant sleep location are included. The recommendations and strength of evidence for each recommendation are published in the accompanying policy statement, "SIDS and Other Sleep-Related Infant Deaths: Updated 2016 Recommendations for a Safe Infant Sleeping Environment," which is included in this issue.
The American Academy of Pediatrics has recommended since 1992 that infants be placed to sleep on their backs to reduce the risk of sudden infant death syndrome (SIDS). Since that time, the frequency of prone sleeping has decreased from >70% to ~20% of US infants, and the SIDS rate has decreased by >40%. However, SIDS remains the highest cause of infant death beyond the neonatal period, and there are still several potentially modifiable risk factors. Although some of these factors have been known for many years (eg, maternal smoking), the importance of other hazards, such as soft bedding and covered airways, has been demonstrated only recently. The present statement is intended to review the evidence about prone sleeping and other risk factors and to make recommendations about strategies that may be effective for further reducing the risk of SIDS. This statement is intended to consolidate and supplant previous statements made by this Task Force.
For families who have experienced the death of a child, their private tragedy is all too often exacerbated by an inappropriate or incompetent professional response. For the professional charged with the responsibility of having to deal with unexpected child deaths, such as a pediatrician, a police officer, or social worker, this title offers guidance on how to respond adequately to this tragic event but also places the subject in a larger social context, examining the history, epidemiology, causes, and contributory factors surrounding the death of a child. The book also covers the prevalence and types of death, the role of the police in an unexpected child death, how to support families, how to undertake a serious case review, and how to prevent child deaths in the future. Part of the prestigious NSPCC Wiley Series in Safeguarding Children - The Multi-Professional Approach.
This study was carried out to determine whether bedding used by infants, who are at either high or low risk for sudden infant death syndrome (SIDS), differs in physical properties favoring rebreathing of exhaled gases.
We compared softness and limitation of carbon dioxide dispersal by bedding, using a mechanical model. A questionnaire was used to describe sociodemographic risk factors and sleep practices; bedding was studied in homes with a model positioned where each infant was found sleeping that morning.
The groups differed with respect to five sociodemographic risk factors (p values all < or = 0.0001). In addition, infants at higher risk were more likely to have been placed to sleep prone (46%, p = 0.02) by parents who were less likely to be aware of the risk associated with the prone position (62% aware, p = 0.005). Infants at higher risk had softer bedding (p < 0.0001, 54.1+/-17.2 cm2 vs 33.7+/-7.7 cm2 in contact with model), which caused more limitation of carbon dioxide dispersal (p = 0.008; CO2 retained, 0.60%+/-0.15% vs 0.34%+/-0.05%).
A series of infants who are at high risk for SIDS because of sociodemographic factors more often sleep on bedding that has physical properties favoring rebreathing, and their parents are less often aware of the risk associated with prone sleeping.
Prone sleeping position, use of soft mattresses and head covering by bedclothes are known risk factors for sudden infant death syndrome (SIDS). Rebreathing carbon dioxide (CO(2) ) may be a possible mechanism or a confounding factor of SIDS.
To compare the aeration properties of a new concept of infant sleeping surface (Net) to three commercial mattresses advertised to improve aeration and to two standard infant mattresses.
Two experiments were performed: (I) A container (head box), filled with 7% CO(2) mixture, was opened to the mattress to allow gas mixture to passively diffuse outside and equilibrate with the surrounding room air. (II) Simulation of normal breathing of an infant, using a unidirectional reciprocal syringe, to determine CO(2) accumulation within the head box.
CO(2) concentrations in the head box were continuously measured until CO(2) levels fell below 1% or for 5 min (experiment I), or until CO(2) accumulation levels plateaued or for 6 min (experiment II).
The Net had a significantly faster rate of CO(2) elimination (88.5 ± 4.6 and 91.9 ± 0.9 sec, Net alone and when covered with a sheet, respectively) compared to 238.3 ± 14.2 sec to 387.8 ± 7.9 sec for the other mattresses (P < 0.001). Only the Net was able to prevent CO(2) accumulation with maximal CO(2) levels (0.56 ± 0.03% and 1.16 ± 0.05%; Net alone and when covered with a sheet, respectively) significantly lower than the range of 4.6-6.3% for the other mattresses (P < 0.001).
The new sleeping surface exhibited significantly better aeration properties in dispersing CO(2) and in preventing its accumulation.
Background:
Parent-infant bed-sharing is a common practice in Western post-industrial nations with up to 50% of infants sleeping with their parents at some point during early infancy. However, researchers have claimed that infants may be at risk of suffocation or sudden infant death syndrome related to airway covering or compression in the bed-sharing environment. To further understand the role of airway covering and compression in creating risks for bed-sharing infants, we report here on a sleep-lab trial of two infant sleep conditions.
Methods:
In a sleep-lab environment 20 infants aged 2-3 months old slept in their parents' bed, and in a cot by the bed, on adjacent nights. Infants' oxygen saturation and heart rate were monitored physiologically while infant and parental behaviours were recorded via ceiling-mounted infra-red cameras. Infants served as their own controls. Continuous 8-h recordings were obtained for covering of infant external airways, levels of infant oxygen saturation, infant heart rate, evidence of parental compression/overlying of infant, circumstances leading up to potential infant airway obstruction, and parental awareness of and responses to infant airway covering.
Results:
The majority of infants (14/20) spent some part of the bed night with their airways (both mouth and nose) covered, compared with 2/20 on the cot night; however, no consistent effect on either oxygen saturation levels or heart rate was revealed, even during prolonged bouts of airway covering. All cases of airway covering were initiated by parents; 70% were terminated by parents, the remainder by infants. Seven bouts of potential compression were observed with parental limbs resting across infant bodies for lengthy periods, however, in only two cases was the full weight of a parental limb resting on an infant, both events lasting less than 15 s, both being terminated by infant movement.
Conclusion:
Although numerous authors have suggested that bed-sharing infants face risks because of airway covering by bed-clothes or parental bodies, the present trial does not lend support to this hypothesis.
We assessed the gas dispersal potential of bedding articles used by 14 infants diagnosed with sudden unexpected infant death at autopsy. Of these cases, eight exhibited FiCO(2) values greater than 10% within 2.5 min, six of which were found prone and two supine. The results demonstrated that these eight beddings had a high rebreathing potential if they covered the babies' faces. We did not, however, take into account in our model the large tissue stores of CO(2). As some bicarbonate pools will delay or suppress the increase of FiCO(2), the time-FiCO(2) graphs of this study are not true for living infants. This model, however, demonstrated the potential gas dispersal ability of bedding. The higher the FiCO(2) values, the more dangerous the situation for rebreathing infants. In addition, FiO(2) in the potential space around the model's face can be estimated mathematically using FiCO(2) values. The FiO(2) graph pattern for each bedding item corresponded roughly to the inverse of the FiCO(2) time course. The FiO(2) of the above eight cases decreased by 8.5% within 2.5 min. Recent studies using living infants placed prone to sleep reported that some babies exhibited larger decreases in FiO(2) than increases observed in FiCO(2). While the decrease of FiO(2) in our model is still theoretical, CO(2) accumulation and O(2) deprivation are closely related. If a striking O(2) deficiency occurs in a short period, babies can lose consciousness before an arousal response is evoked and all infants could be influenced by the poor gas dispersal of bedding; the main cause of sudden death in infancy would thus be asphyxia. When the bedding is soft, the potential for trapping CO(2) seems to be high; however, it is impossible to assess it by appearance alone. We sought to provide some objective indices for the assessment of respiratory compromise in relation to bedding using our model. When a baby is found unresponsive with his/her face covered with poor gas dispersal bedding, we should consider the possibility of asphyxia.
Suffocation by bedclothes became a popular diagnosis in the 1940s but gradually became replaced with the diagnostic label of Sudden Infant Death Syndrome (SIDS). In 1991 a paper purported that, instead of SIDS, pillows filled with polystyrene beads had caused death by rebreathing suffocation; this conclusion was reached on the basis of experiments with anesthetized rabbits breathing through a doll's head that was placed face down on the pillow. Because of the anesthesia, rabbits could not change their face down position. The doll's nares could not collapse, which would have resulted in rapid death due to conventional suffocation. The rabbits required up to 3 hours or more to die of hypercarbia and hypoxia. Studies in normal infants revealed that they turned from the face-down position after only 2 minutes. (The only infant who retained CO2 soon died of a fatal neurologic disorder, with central hypoventilation). Using the rabbit/doll's head and mechanical models, a wide range of bedding was indicted, including cushions, sheepskins, pillows, comforters, foam mattresses, and even simple blankets and sheets as potentially causing fatal rebreathing. Except for the use of pillows in general, as well as mattresses filled with kapok and bark, there has been no epidemiologic support for these indictments.
Twenty to 52% of sudden infant death syndrome (SIDS) victims are found dead with their noses and mouths turned into underlying bedding. Several items of bedding have been shown to increase the risk for SIDS in case-control studies or to be associated with many SIDS deaths in case series. These items of bedding are after limit CO2 dispersal more, and cause more rebreathing of exhaled gases than bedding infrequently associated with SIDS. Rebreathing of exhaled gases may explain some prone deaths, and avoiding rebreathing of these gases is one possible mechanism for the reduction in SIDS when infants avoid prone sleep. Results supporting these statements are reviewed and discussed.
To study factors associated with sudden infant deaths occurring with the external airways (ie, nose and mouth) covered by bedding.
Case-comparison study of infants dying with vs those dying without the external airways covered.
Death-scene investigation and reconstruction at the site of death using an infant mannequin; 18 metropolitan areas.
Caregivers for a consecutive sample of infants who died of sudden infant death syndrome (SIDS). Complete data from 206 of 382 eligible cases.
Among infants dying suddenly and unexpectedly, an analysis of whether sociodemographic risk factors for SIDS, sleep practices, or bedding increased the risk of dying with the external airways covered.
Data were analyzed by using univariate and 2 types of multivariate risk analysis, logistic regression and latent class. Of the victims, 59 (29%) were found with the external airways covered. Conventional risk factors for SIDS did not affect the risk of death with the external airways covered. Factors increasing the risk of death with the external airways covered included prone sleep position (odds ratio [OR], 2.86) and using soft bedding (OR, 5.28), such as comforters (OR, 2.46) and pillows (OR, 3.31). Infants at low risk for death with the external airways covered slept in the prone position, but rarely on a pillow, comforter, or other bedding that allowed a pocket to form beneath the face. All 9 infants who were positioned supine or on one side for sleep and found with the external airways covered had turned and were found dead in the prone position.
Sudden infant deaths with the external airways covered were common in the United States when most infants slept prone. Soft bedding, including pillows and comforters, increased the risk that an infant who died would be found with the external airways covered. Therefore, these items should not be placed near infants, regardless of the sleep position.
We assessed some Japanese bedding on the assumption of the effects of air trapping using an infant mannequin. The change of CO2 concentration in the airway of a mannequin head placed on bedding was continuously monitored using a CO2 analyzer during simulated breathing. To compare the level of CO2 dispersal among different items of bedding, CO2 half time (t1/2) values were used. The t1/2 values were calculated by measuring the time required for the expired percent CO2 to reach 1/2 the initial percent end-tidal PCO2. We also measured softness and resistance to airflow (R) of the same items. As for the bedding, 4 types of futon and several types of bottom sheets/towels were combined. The t1/2 value in supine position was 9.8 seconds. When the model was placed prone on futon, the t1/2 values increased to 14.1 seconds (hard mattress type)--17.2 seconds (soft cotton-like futon). With respect to present Japanese baby futon (hard mattress type), there may be a relatively low potential for rebreathing to occur, compared with soft futon. In every case, the t1/2 value was prolonged by the use of a towel spread on the futon. CO2 dispersal may depend not only on the softness of the futon, but also on the combination of bottom sheet/towel and mattress. There was no relationship between R values and t1/2 values. The potential of rebreathing increased in face down position among all bedding, and supine position was the best CO2 dispersal position.
This article offers one institution's approach to implementation of the recommendations for infant sleep positioning as set forth by the American Academy of Pediatrics. The guidelines are directed toward healthy infants in the first year of life, a population not always encountered
by the neonatal nurse. The guidelines focus on supine sleep position and the minimization of additional bedding, both of which can be challenging when contrasted with accomplishing supportive positioning and the goals of developmentally supportive care for ill or preterm infants. A multidisciplinary
task force was formed to consider this challenge. The outcome is an evidence-based policy that is presented as an example for other clinicians. The policy addresses the following major components: sleep position with specific clinical exceptions, the use of bedding materials, play position
during awake states, and parent education with preparation for discharge. The article also outlines the process by which the task force plans to implement and evaluate necessary practice changes.
The mechanisms underlying the sudden infant death syndrome (SIDS) appear to have origins in the fetal environment resulting in neural damage which later compromises responses to breathing or blood pressure challenges during sleep. The deficits appear to involve alterations in neurotransmitter receptors within regions involved in chemoreception and cardiovascular control. SIDS risk is enhanced by pre- and postnatal nicotine exposure, and possibly by hypoxic experiences. The prone sleeping position plays a significant role in risk, as do head positions that minimize facial escape from enclosed spaces; elevated body temperature may also be a factor. Compensatory mechanisms, including diminished gasping ability, relative failure to arouse to a safer state, or a failure to recruit respiratory efforts to overcome a blood pressure loss have been the object of recent research efforts. The findings suggest that the fatal event involves a neurally-compromised infant, circumstances that challenge vital physiology, most likely during sleep, at a particular developmental period.
The physiological effects on an infant of repeatedly sleeping in an environment consisting of a mixture of exhaled air and fresh air is examined. It is found that adaptation can be predicted. A possible outcome of the adaptation is shown to be the development of hypoxia when the conditions change during sleep from a state with carbon dioxide contamination of inspired air to one without. This hypoxia can be associated with apnoea: this apnoea can provide an explanation for some instances of sudden infant death. This explanation is consistent with the known epidemiology and environmental associations of a proportion of sudden infant death syndrome. Safety precautions for the prevention of re-breathing are given.
Soft bedding increases the risk for death among prone infants. We compared the softness of beds and bedding and infant sleep position for infants sleeping alone and for those bed sharing.
Questionnaires were used to record the bedding and sleep practices of 218 consecutive African American infants. Enrollment was prospective. Mechanical models were used in the homes of a subgroup to measure the softness of bedding and its propensity to cause rebreathing. Results were compared by using the Student t test, Mann-Whitney U test, and chi(2) analysis.
In a cross-sectional sample of infants, at 8.2 +/- 3.3 weeks of age, 61% (133 of 218) had bed shared > or =1 of the previous 14 nights and 48.6% (106 of 218) had bed shared the night before. Breast-feeding rates were not different for bed sharers and those sleeping alone. The rates of maternal smoking for both groups were low (13.6% vs 11.8%). Comforters, pillows, and waterbeds were more commonly used beneath bed-sharing infants. Bed sharers were twice as likely to habitually be placed prone for sleep (18% vs 9%). In the subgroup studied in their homes (13 bed sharing, 19 alone), the shared beds were softer (P <.0001) and could cause more rebreathing (P =.007).
Infants at increased risk for sudden infant death syndrome, by sociodemographic criteria, who also bed share are more likely to sleep prone and to use softer beds. These findings may explain part of the risk associated with bed sharing among US infants, a risk that appears to be independent of the effects of maternal smoking.
Sudden infant death syndrome (SIDS) accounts for the largest number of deaths during the first year of life in developed countries. The possible causes of SIDS are numerous and, to date, there is no adequate unifying pathological explanation for SIDS. Epidemiological studies have played a key role in identifying risk factors, knowledge of which has underpinned successful preventive programmes. This review critically assesses information on the main risk factors and causal hypotheses put forward for SIDS, focusing on research published since 1994. The overall picture that emerges from this review is that affected infants are not completely normal in development, but possess some inherent weakness, which may only become obvious when the infant is subjected to stress. Initially there may be some minor impairment or delay in development of respiratory, cardiovascular or neuromuscular function. None of these is likely to be sufficient, in isolation, to cause death and, provided the infant survives the first year of life, may no longer be of any significance. However, when a compromised infant is confronted with one or more stressful situations, several of which are now clearly identified as risk factors, and from which the majority of infants would normally escape, the combination may prove fatal.
Infants who sleep prone and face down on soft bedding are particularly vulnerable for sudden infant death syndrome. It has been suggested that 1 mechanism of death in this situation involves rebreathing of expired air. Many infants tolerate rebreathing while lying prone face down for long periods with stable saturations. Others occasionally have rapid desaturations and may require intervention to terminate rebreathing. The present study had 3 objectives: 1) to determine the frequency of rapid desaturations in a large group of healthy infants, 2) to elucidate the mechanism of these desaturations, and 3) to determine the timing of these events during periods of rebreathing.
We studied respiratory tracings and videotapes of 56 healthy 1- to 6-month-old infants who were sleeping face down and rebreathing on soft bedding in our laboratory. We compared the frequency of desaturations during rebreathing and nonrebreathing periods. We measured respiratory frequency and apnea occurrence before desaturation and nonrebreathing control episodes. We also measured minute ventilation during steady state before desaturation and just before desaturation.
There were 25 desaturation episodes in infants while rebreathing, occurring in 11 (19.6%) of the 56 infants. Episodes were significantly more frequent during rebreathing than during nonrebreathing periods. Three desaturation episodes reached <85%; 2 required intervention to terminate rebreathing. The respiratory frequency was not different between nonrebreathing control and desaturation episodes. Brief apneas were significantly more frequent preceding desaturation than control episodes (44% vs 4%). Just before episodes, there was a transient decrease in minute volume despite increasing inspired carbon dioxide in 3 episodes. There was evidence of partial or complete pharyngeal airway obstruction in 3 episodes. Thirty-six percent of all episodes were immediately preceded by behavioral arousal.
Rebreathing in prone sleeping infants is associated with an increased frequency of episodic desaturations. Desaturation may result from respiratory pattern changes such as brief apneas often associated with evidence of behavioral arousal or failure to increase ventilation in the face of rising inspired carbon dioxide, also associated with behavioral arousal.
Rebreathing is thought to be associated with sudden infant death syndrome (SIDS). The aim of the present study was to evaluate the rebreathing potential of different types of Japanese infant bedding.
The rebreathing potential of various combinations of infant bedding was measured using a mechanically simulated breathing model. The types of bedding included five types of mattresses, four types of o-nesyo sheets (waterproof sheets) and a towel. The half-life of the expiratory CO2 concentration, t1/2-value was calculated as the index of the rebreathing potential. The softness of the bedding was also measured.
There was a moderate proportional correlation between the t1/2-value and the softness (correlation coefficient = 0.509). When a new hard infant mattress was used, the t1/2-values were 13.6-14.1 s, and when o-nesyo sheet was added, the values were 14.1-16.2 s. When other mattresses were used with the o-nesyo sheet, the values were 14.1-19.2 s. Adding a towel onto the bedding, the t1/2-value (18.5-22.3 s) was prolonged without exception.
It is difficult to estimate the rebreathing potential of the bedding on the basis its appearance or its softness. All infants should be placed on appropriate bedding in case they turn to a prone-sleeping position. Our recommendations to avoid rebreathing are as follows: (i) a new hard mattress specifically designed for babies should be used; (ii) a towel should not be used; (iii) an o-nesyo sheet may be used with a new hard infant mattress if necessary.
To determine the role of heat stress in sudden infant death syndrome (SIDS) by examining the SIDS rates during periods of extreme environmental temperatures in a period when most infants were placed prone for sleep.
A retrospective study of SIDS rates and mortality rates attributable to excessive environmental heat in relationship to climatologic temperature was performed. Data were collected for each of 454 counties in 4 states (Arkansas, Georgia, Kansas, and Missouri) from May 1 to September 30, 1980, and were then summed to yield the mortality rates for each 5 degrees F (2.8 degrees C) temperature range.
chi2 analyses revealed significant relationships for heat-related mortality rates and both the maximal daily temperature and mean daily temperature but demonstrated no such relationships for SIDS rates. No association between SIDS rates and heat-related mortality rates was found with Spearman's ranked correlation, for either the maximal daily temperature or the mean daily temperature.
On the basis of our findings of no significant association between SIDS and either measure of temperature during periods of high heat stress-related death rates, it seems unlikely that the heat stress associated with the combination of prone sleep positions and elevated environmental temperatures has a significant role in the development of SIDS.
Several studies have found that back- or side-sleeping infants who are inexperienced in prone sleeping are at much higher risk for sudden infant death syndrome (SIDS) when they turn to prone or are placed prone for sleep compared with infants who normally sleep prone. Moreover, such inexperienced infants are more likely to be found in the face-down position at death after being placed prone compared with SIDS infants who are experienced in prone sleeping. We hypothesized that lack of experience in prone sleeping is associated with increased difficulty in changing head position to avoid an asphyxiating sleep environment.
We studied 38 healthy infants while they slept prone. Half of these were experienced and half were inexperienced in prone sleeping. To create a mildly asphyxiating microenvironment, we placed infants to sleep prone with their faces covered by soft bedding. We recorded inspired CO2 (CO2I), electrocardiogram, and respiration, and we videotaped head movements. Also, we assessed gross motor development (Denver Development Scale).
When sleeping prone, with their faces covered by bedding, all infants experienced mild asphyxia as a result of rebreathing. All aroused and attempted escape from this environment. Infants used 3 stereotyped head-repositioning strategies. The least effective was nuzzling into the bedding with occasional brief head lifts. More effective were head lifts combined with a head turn. Some infants, however, could turn only to 1 side, right or left. Infants who were inexperienced in prone sleeping had less effective protective behaviors than experienced infants. Infant age did not correlate with efficacy of protective behaviors. Infants who were experienced in prone sleep had advanced gross motor development compared with inexperienced infants.
Infants who are inexperienced in prone sleeping have decreased ability to escape from asphyxiating sleep environments when placed prone. These observations potentially explain the increased risk associated with prone sleep in infants who are inexperienced. The increased occurrence of the face-down position in such infants is also potentially explained. These findings suggest that airway protective behaviors may be acquired through the mechanism of operant conditioning (learning).
Rebreathing is a model for the relationship between a prone sleeping position and sudden infant death syndrome. This study used a mechanical simulation model to establish the relationship between types of bedding and rebreathing potential for an infant placed prone (face down) at different postnatal ages. The infant mannequin was connected to a respirator set to deliver physiologically appropriate combinations of tidal volume (V(T)) and respiratory rates (RR) across a range of postnatal ages (0-18 months). Before measurements were made, CO(2) flow was regulated to 5+/-0.1% of end-tidal PCO(2) (EtCO(2)). After the model was placed in a prone position, any increase in the fractional concentration of inspired CO(2) (FiCO(2)) was measured. FiCO(2) increased immediately and rapidly, and reached a maximum value within a few minutes. The maximum FiCO(2) ranged from under 2% to over 10%, depending on the bedding. FiCO(2) was also affected by V(T) and RR. This model is not applicable to actual infants because of the large tissue stores of CO(2) in infants; however, it is useful for evaluation of gas diffusibility of bedding and will simplify the investigation of sleeping environments when a baby is found dead with its face covered by soft bedding. In general, the higher the FiCO(2), the greater the rebreathing potential. Theoretically, considering the paucity of body stores of O(2), changes in FiO(2) would be affected not by changes in FiCO(2), but by CO(2) production and gas movement around the infant's face. The rapid decrease of FiO(2) is approximated at the inverse of the FiCO(2) timecourse, suggesting the significance of not only CO(2) accumulation but also O(2) deprivation in the potential space around the baby's face.
An electrophoretic protocol previously used for the separation of rat myosin heavy chain (MHC) isoforms was slightly modified to improve the separation of human MHC isoforms in both large and minigel systems. The addition of reducing agents (beta-mercaptoethanol or dithiothreitol) to the top running buffer (TRB) radically improved separated MHC isoform resolution and the intensity of electrophoretic runs lasting longer than 5 h. In minigel systems, the MHC isoforms could be separated in as little as 5 h. The improved resolution of bands with the inclusion of reducing agents to the TRB facilitated the identification of clear boundaries for densitometric quantification of relative MHC isoform content, particularly for MHC IIa and MHC IIx. No significant effect of these reducing agents added to the TRB was observed for runs lasting only 100 min. Thus the inclusion of reducing agents in the TRB is essential for long electrophoretic runs, usually when separating large molecular mass proteins.
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